The pertussis hypothesis: Bordetella pertussis colonization in the pathogenesis of Alzheimer’s disease
While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immun...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Rubin, Keith [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017transfer abstract |
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| Schlagwörter: |
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| Umfang: |
13 |
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| Übergeordnetes Werk: |
Enthalten in: Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center - Clark, Leon G. ELSEVIER, 2016, experimental and clinical, München |
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| Übergeordnetes Werk: |
volume:222 ; year:2017 ; number:2 ; pages:228-240 ; extent:13 |
| Links: |
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| DOI / URN: |
10.1016/j.imbio.2016.09.017 |
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ELV040346331 |
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| 245 | 1 | 4 | |a The pertussis hypothesis: Bordetella pertussis colonization in the pathogenesis of Alzheimer’s disease |
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| 520 | |a While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD. | ||
| 520 | |a While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD. | ||
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10.1016/j.imbio.2016.09.017 doi GBV00000000000097A.pica (DE-627)ELV040346331 (ELSEVIER)S0171-2985(16)30384-9 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Rubin, Keith verfasserin aut The pertussis hypothesis: Bordetella pertussis colonization in the pathogenesis of Alzheimer’s disease 2017transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD. While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD. NADPH Elsevier CDC Elsevier BBB Elsevier PS Elsevier CNS Elsevier DPT Elsevier kDa Elsevier mRNA Elsevier cAMP Elsevier BP Elsevier Aβ Elsevier HSV-1 Elsevier GRK2 Elsevier SCBPC Elsevier BACE-1 Elsevier CSF Elsevier GA Elsevier APOE Elsevier Th1 Elsevier NFT Elsevier Th17 Elsevier US Elsevier AD Elsevier BDNF Elsevier aPV Elsevier MS Elsevier PKA Elsevier IL-1β Elsevier ER Elsevier IL-6 Elsevier sAPPα Elsevier GABAB Elsevier GSK3β Elsevier TNF-α Elsevier AβPP Elsevier wPV Elsevier GLUT4 Elsevier CVO Elsevier CGRP Elsevier ATP Elsevier PCR Elsevier NAD+ Elsevier Glazer, Steven oth Enthalten in Elsevier Clark, Leon G. ELSEVIER Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center 2016 experimental and clinical München (DE-627)ELV013869728 volume:222 year:2017 number:2 pages:228-240 extent:13 https://doi.org/10.1016/j.imbio.2016.09.017 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_40 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 222 2017 2 228-240 13 045F 570 |
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10.1016/j.imbio.2016.09.017 doi GBV00000000000097A.pica (DE-627)ELV040346331 (ELSEVIER)S0171-2985(16)30384-9 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Rubin, Keith verfasserin aut The pertussis hypothesis: Bordetella pertussis colonization in the pathogenesis of Alzheimer’s disease 2017transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD. While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD. NADPH Elsevier CDC Elsevier BBB Elsevier PS Elsevier CNS Elsevier DPT Elsevier kDa Elsevier mRNA Elsevier cAMP Elsevier BP Elsevier Aβ Elsevier HSV-1 Elsevier GRK2 Elsevier SCBPC Elsevier BACE-1 Elsevier CSF Elsevier GA Elsevier APOE Elsevier Th1 Elsevier NFT Elsevier Th17 Elsevier US Elsevier AD Elsevier BDNF Elsevier aPV Elsevier MS Elsevier PKA Elsevier IL-1β Elsevier ER Elsevier IL-6 Elsevier sAPPα Elsevier GABAB Elsevier GSK3β Elsevier TNF-α Elsevier AβPP Elsevier wPV Elsevier GLUT4 Elsevier CVO Elsevier CGRP Elsevier ATP Elsevier PCR Elsevier NAD+ Elsevier Glazer, Steven oth Enthalten in Elsevier Clark, Leon G. ELSEVIER Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center 2016 experimental and clinical München (DE-627)ELV013869728 volume:222 year:2017 number:2 pages:228-240 extent:13 https://doi.org/10.1016/j.imbio.2016.09.017 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_40 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 222 2017 2 228-240 13 045F 570 |
| allfields_unstemmed |
10.1016/j.imbio.2016.09.017 doi GBV00000000000097A.pica (DE-627)ELV040346331 (ELSEVIER)S0171-2985(16)30384-9 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Rubin, Keith verfasserin aut The pertussis hypothesis: Bordetella pertussis colonization in the pathogenesis of Alzheimer’s disease 2017transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD. While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD. NADPH Elsevier CDC Elsevier BBB Elsevier PS Elsevier CNS Elsevier DPT Elsevier kDa Elsevier mRNA Elsevier cAMP Elsevier BP Elsevier Aβ Elsevier HSV-1 Elsevier GRK2 Elsevier SCBPC Elsevier BACE-1 Elsevier CSF Elsevier GA Elsevier APOE Elsevier Th1 Elsevier NFT Elsevier Th17 Elsevier US Elsevier AD Elsevier BDNF Elsevier aPV Elsevier MS Elsevier PKA Elsevier IL-1β Elsevier ER Elsevier IL-6 Elsevier sAPPα Elsevier GABAB Elsevier GSK3β Elsevier TNF-α Elsevier AβPP Elsevier wPV Elsevier GLUT4 Elsevier CVO Elsevier CGRP Elsevier ATP Elsevier PCR Elsevier NAD+ Elsevier Glazer, Steven oth Enthalten in Elsevier Clark, Leon G. ELSEVIER Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center 2016 experimental and clinical München (DE-627)ELV013869728 volume:222 year:2017 number:2 pages:228-240 extent:13 https://doi.org/10.1016/j.imbio.2016.09.017 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_40 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 222 2017 2 228-240 13 045F 570 |
| allfieldsGer |
10.1016/j.imbio.2016.09.017 doi GBV00000000000097A.pica (DE-627)ELV040346331 (ELSEVIER)S0171-2985(16)30384-9 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Rubin, Keith verfasserin aut The pertussis hypothesis: Bordetella pertussis colonization in the pathogenesis of Alzheimer’s disease 2017transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD. While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD. NADPH Elsevier CDC Elsevier BBB Elsevier PS Elsevier CNS Elsevier DPT Elsevier kDa Elsevier mRNA Elsevier cAMP Elsevier BP Elsevier Aβ Elsevier HSV-1 Elsevier GRK2 Elsevier SCBPC Elsevier BACE-1 Elsevier CSF Elsevier GA Elsevier APOE Elsevier Th1 Elsevier NFT Elsevier Th17 Elsevier US Elsevier AD Elsevier BDNF Elsevier aPV Elsevier MS Elsevier PKA Elsevier IL-1β Elsevier ER Elsevier IL-6 Elsevier sAPPα Elsevier GABAB Elsevier GSK3β Elsevier TNF-α Elsevier AβPP Elsevier wPV Elsevier GLUT4 Elsevier CVO Elsevier CGRP Elsevier ATP Elsevier PCR Elsevier NAD+ Elsevier Glazer, Steven oth Enthalten in Elsevier Clark, Leon G. ELSEVIER Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center 2016 experimental and clinical München (DE-627)ELV013869728 volume:222 year:2017 number:2 pages:228-240 extent:13 https://doi.org/10.1016/j.imbio.2016.09.017 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_40 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 222 2017 2 228-240 13 045F 570 |
| allfieldsSound |
10.1016/j.imbio.2016.09.017 doi GBV00000000000097A.pica (DE-627)ELV040346331 (ELSEVIER)S0171-2985(16)30384-9 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Rubin, Keith verfasserin aut The pertussis hypothesis: Bordetella pertussis colonization in the pathogenesis of Alzheimer’s disease 2017transfer abstract 13 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD. While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD. NADPH Elsevier CDC Elsevier BBB Elsevier PS Elsevier CNS Elsevier DPT Elsevier kDa Elsevier mRNA Elsevier cAMP Elsevier BP Elsevier Aβ Elsevier HSV-1 Elsevier GRK2 Elsevier SCBPC Elsevier BACE-1 Elsevier CSF Elsevier GA Elsevier APOE Elsevier Th1 Elsevier NFT Elsevier Th17 Elsevier US Elsevier AD Elsevier BDNF Elsevier aPV Elsevier MS Elsevier PKA Elsevier IL-1β Elsevier ER Elsevier IL-6 Elsevier sAPPα Elsevier GABAB Elsevier GSK3β Elsevier TNF-α Elsevier AβPP Elsevier wPV Elsevier GLUT4 Elsevier CVO Elsevier CGRP Elsevier ATP Elsevier PCR Elsevier NAD+ Elsevier Glazer, Steven oth Enthalten in Elsevier Clark, Leon G. ELSEVIER Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center 2016 experimental and clinical München (DE-627)ELV013869728 volume:222 year:2017 number:2 pages:228-240 extent:13 https://doi.org/10.1016/j.imbio.2016.09.017 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO GBV_ILN_40 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 222 2017 2 228-240 13 045F 570 |
| language |
English |
| source |
Enthalten in Pyostomatitis vegetans (PSV)-pyodermatitis vegetans (PDV): A clinicopathologic study of 7 cases at a tertiary referral center München volume:222 year:2017 number:2 pages:228-240 extent:13 |
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While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD. |
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While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD. |
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While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV040346331</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625231620.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2017 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.imbio.2016.09.017</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBV00000000000097A.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV040346331</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0171-2985(16)30384-9</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">570</subfield><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">570</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">333.7</subfield><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">43.12</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">43.13</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.13</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Rubin, Keith</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="4"><subfield code="a">The pertussis hypothesis: Bordetella pertussis colonization in the pathogenesis of Alzheimer’s disease</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2017transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">13</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. We conclude by assessing the evidence for causation against the Bradford Hill criteria, and advocate for further investigation into the potential role of BP in the etiology of AD.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">While a number of endogenous risk factors including age and genetics are established for Alzheimer’s disease (AD), identification of acquired, potentially preventable or treatable causes, remains limited. In this paper, we review three epidemiologic case studies and present extensive biologic, immunologic and anatomic evidence to support a novel hypothesis that Bordetella pertussis (BP), the bacterium better known to cause whooping cough, is an important potential cause of AD. Cross-cultural documentation of nasopharyngeal subclinical BP colonization reflecting BP-specific mucosal immunodeficiency, proximate anatomy of intranasal mucosal surfaces to central nervous system (CNS) olfactory pathways, and mechanisms by which BP and BP toxin account for all hallmark pathology of AD are reviewed, substantiating biologic plausibility. Notably, respiratory BP infection and BP toxin secreted from subclinical BP colonization can account for the initiation and accumulation of amyloid β plaques and tau tangles. Additional mechanisms consistent with the immunobiologic effects of subclinical BP colonization include microglial activation and inflammation, atrophy and neurodegeneration, excitotoxicity, distinctive anatomic distribution and sequential spread of disease, impaired glucose utilization, and other characteristic CNS pathology of AD. 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